Previous studies on UV-induced tumors have clearly demonstrated that these tumors express multiple tumor associated antigens (TAA) and that these different antigens under varying circumstances can selectively activate either the regulatory or the effector pathways of immune response. This research program will now further pursue this model system in depth, with the aim of identifying the different tumor specific antigens and determining the mechanisms by which they selectively activate suppressor or effector immune responses. A major part of the present proposal is to develop monoclonal reagents that will clearly identify the different tumor antigens on individual UV induced tumors. Two parallel approaches will be applied to this problem, involving the generation of hybridoma derived monoclonal antibodies against UV induced tumor antigens and, secondly, the development of cloned continuous T cell lines of either cytotoxic or helper type which are reactive against antigens on the same tumor. A battery of such reagents of both types will thus be developed which in turn will be used to monitor the isolation of the individual tumor specific antigens, and to determine whether the same antigens can selectively invoke both humoral and T cell immune responsiveness. This research program will also involve further transplantation studies with emphasis on elucidating more clearly the nature of UV-induced suppressor cells. This work will include an in-depth phenotypic characterization of the antigens expressed by the suppressor cells using our various rat monoclonal antibodies to murine differentiation antigens, as well as in vitro UV irradiation of various cell types to investigate the source and nature of antigens which elicit suppression. The ultimate aim is to relate the ability of the individual antigens to their immunoregulatory or immunoeffector stimulatory properties. Such a model system may ultimately provide the ideal model for characterization of the types of tumor antigens that in man may be selectively used for activation of effector immune responses in immunotherapy protocols.